The success of estrogen and estrogen-like drugs in combating osteoporosis in postmenopausal women may indicate that estrogen:
High-Yield Explanation
Estrogens directly regulate osteoblasts and increase the synthesis of type I collagen, osteocalcin, osteopontin, osteonectin, alkaline phosphatase, and other markers of differentiated osteoblasts. Estrogens also increase osteocyte survival by inhibiting apoptosis. However, the major effect of estrogens is to decrease the number and activity of osteoclasts. Much of the action of estrogens on osteoclasts appears to be mediated by altering cytokine (both paracrine and autocrine) signals from osteoblasts. Estrogens decrease osteoblast and stromal cell production of the osteoclast-stimulating cytokines interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)- and increase the production of IGF-1, bone morphogenic protein (BMP)-6, and transforming growth factor (TGF) Beta which are antiresorptive. Ref: Levin E.R., Hammes S.R. (2011). Chapter 40. Estrogens and Progestins. In L.L. Brunton, B.A. Chabner, B.C. Knollmann (Eds), Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e.